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Background: Fried food has increased in popularity worldwide. However, deep frying can increase the production of peroxidative toxins in food, which might be harmful to fetal development. The antioxidative effect of vitamin D3 (VD3) has been reported previously., Objectives: This study aimed to explore how maternal VD3 supplementation in an oxidized-oil diet during gestation affects fetal antioxidative ability and development., Methods: Pregnant mice were randomly assigned into 3 groups: Control group (diet with fresh soybean oil), OSO group [diet with oxidized soybean oil (OSO)], and OSOV group (diet with OSO and 10,000 IU/Kg VD3). Mice were fed with the corresponding diet during gestation. On day 16.5 of gestation, the placenta and fetus were harvested to analyze antioxidative status., Results: Maternal oxidized-oil diet during gestation significantly reduced placental vessel abundance, labyrinth zone area, and fetal body weight. However, dietary VD3 supplementation prevented these negative effects of oxidized-oil diet. Maternal intake of oxidized-oil diet increased serum concentrations of malondialdehyde, total-nitric oxide synthase, and inducible nitric oxide synthase, whereas VD3 supplementation showed a protection effect on it. Additionally, maternal VD3 supplementation increased the levels of antioxidative enzymes and the nuclear translocation of nuclear factor erythroid 2-related factor 2 (NRF2), thereby protecting placenta and fetus from apoptosis and oxidative stress caused by an oxidized-oil diet. The gene expression and protein levels of a fatty acid transporter solute carrier family 27 member 1 in the fetal liver were increased by maternal VD3 supplementation under oxidized-oil diet. Notably, NRF2 could be co-immunoprecipitated with the VD receptor in the placenta., Conclusions: Maternal VD3 supplementation could protect fetus from oxidized-oil diet induced developmental impairment by alleviating oxidative stress in the placenta and fetus through the VD receptor/NRF2 pathway, at least partially. Thus, ensuring adequate levels of VD3 through supplementation is often critical during pregnancy., (Copyright © 2024 American Society for Nutrition. Published by Elsevier Inc. All rights reserved.)

Neuronal loss and impairment of oxidative metabolism are frequently observed in aging associated neurodegenerative diseases. Thiamine deficiency (TD) induces the region selective neuronal loss in the brain, which has been used to model neurodegeneration, accompanied by mild impairment of oxidative metabolism. C57BL/6 mice were commonly used animals for TD experiments; however, the individual variations among C57BL/6 mice in response to TD limited the consistence of brain pathology. The senescence accelerated prone 8 (SAMP8) mouse strain exhibits age-related morphological changes in the brain and deficits in learning and memory. In this study, we compared the effects of TD on SAMP8 mice, senescence accelerated resistant 1 (SAMR1) mice and C57BL/6 mice. TD-induced body weight loss in SAMP8 mice was much greater than in SAMR1 and C57BL/6 mice. In addition, earlier and more severe loss of neurons in the submedial thalamic nucleus (SmTN) of the thalamus was detected in the SAMP8 mice. After 8 days of TD (TD8), the loss of NeuN-positive neurons in the SmTN of SAMP8, SAMR1 and C57BL/6 mice was 65%, 50%, and 36%, respectively. TD also caused accumulation of amyloid precursor protein (APP) in the thalamus. After TD10, APP immunoreactivity in the thalamus of SAMP8 was much more intense than that of SAMR1 and C57BL/6 mice. These results suggest that SAMP8 mice are sensitive to TD and therefore offer a useful model for studying aging related neurodegeneration caused by the impairment of oxidative metabolism.

Dietary oxidized fat contains harmful materials such as hydrogen peroxide and malondialdehyde (MDA). Excessive oxidized fat intake during pregnancy and lactation not only leads to maternal body injury but also damages offspring health. Our previous study demonstrated that vitamin D (VD) had antioxidative capability in sows. This study was conducted to investigate the effect of maternal VD and inulin supplementation in oxidized oil diet on the growth performance and oxidative stress of their offspring. Sixty 5-month-old C57BL/6N female mice were randomly divided into five groups: Control group (basal diet, n = 12), OF group (oxidized-soybean-oil-replaced diet, n = 12), OFV group (oxidized-soybean-oil-replaced diet + 7000 IU/kg VD, n = 12), OFI group (oxidized-soybean-oil-replaced diet + 5% inulin, n = 12) and OFVI group (oxidized-soybean-oil-replaced diet + 7000 IU/kg VD + 5% inulin, n = 12). Mice were fed with the respective diet during pregnancy and lactation. The offspring were then slaughtered on day 21 of age at weaning. Results showed that a maternal oxidized oil diet impaired body weight and liver weight gain of offspring during lactation compared to the control group, while maternal VD, inulin or VD and inulin mixture supplementation reversed this effect. In addition, the activity of T-AOC in the liver of offspring was lower in the OF group than that in the control group, but could be restored by maternal VD and inulin mixture supplementation. Furthermore, the gene expression of both proinflammatory and anti-inflammatory cytokines, such as Il-6, Tnfα and Il-10, in offspring liver were downregulated by a maternal oxidized oil diet compared with the control group, but they were restored by maternal VD or VD and inulin mixture supplementation. The expressions of Vdr and Cyp27a1 were decreased by a maternal oxidized oil diet compared with the control group, while they could be increased by VD or VD and inulin mixture supplementation. Conclusion: maternal oxidized oil diet intake could impair the growth performance by inducing oxidative stress, but this can be relieved by maternal VD and inulin supplementation. [ABSTRACT FROM AUTHOR]

Abstract: Thiamine pyrophosphate (TPP) and the activities of thiamine-dependent enzymes are reduced in Alzheimer''s disease (AD) patients. In this study, we analyzed the relationship between thiamine deficiency (TD) and amyloid precursor protein (APP) processing in both cellular and animal models of TD. In SH-SY5Y neuroblastoma cells overexpressing APP, TD promoted maturation of β-site APP cleaving enzyme 1 (BACE1) and increased β-secretase activity which resulted in elevated levels of β-amyloid (Aβ) as well as β-secretase cleaved C-terminal fragment (β-CTF). An inhibitor of β-secretase efficiently reduced TD-induced up-regulation of Aβ and β-CTF. Importantly, thiamine supplementation reversed the TD-induced alterations. Furthermore, TD treatment caused a significant accumulation of reactive oxygen species (ROS); antioxidants suppressed ROS production and maturation of BACE1, as well as TD-induced Aβ accumulation. On the other hand, exogenous Aβ1–40 enhanced TD-induced production of ROS. A study on mice indicated that TD also caused Aβ accumulation in the brain, which was reversed by thiamine supplementation. Taken together, our study suggests that TD could enhance Aβ generation by promoting β-secretase activity, and the accumulation of Aβ subsequently exacerbated TD-induced oxidative stress. [Copyright &y& Elsevier]

Ochratoxin A (OTA) is a mycotoxin ubiquitous in feeds and foodstuffs. The water-insoluble pentacyclic triterpene bioactive compound, ursolic acid (UA), is widespread in various cuticular waxes of edible fruits, food materials, and medicinal plants. Although studies have reported that oxidative stress was involved in both the nephrotoxicity of OTA and the renoprotective function of UA, the role of stress-responsive Lon protease 1 (Lonp1) in the renoprotection of UA against OTA is still unknown. In this study, cell viability, reactive oxygen species (ROS) production, and several proteins' expressions of human embryonic kidney 293T (HEK293T) cells in response to UA, OTA, and/or Lonp1 inhibitor CDDO-me treatment were detected to reveal the protective mechanism of UA against OTA-induced renal cytotoxicity. Results indicated that a 2 h-treatment of 1 μM UA could significantly alleviate the ROS production and cell death induced by a 24 h-treatment of 8 μM OTA in HEK293T cells (P < 0.05). Compared with the control, the protein expressions of Lonp1, Aco2 and Hsp75 were significantly inhibited after 8 μM OTA treating for 24 h (P < 0.05), which could be notably reversed by the pre-treatment and post-treatment of 1 μM UA (P < 0.05). The protein expressions of Lonp1, Aco2 and Hsp75 were inhibited by the addition of CDDO-me. The three protein expression trends were similar before and after the addition of CDDO-me. In conclusion, OTA could inhibit the expression of Lonp1, suppressing Aco2 and Hsp75 as a result, thereby activating ROS and inducing cell death in HEK293T cells, which could be alleviated by UA pre-treatment. Image 1 • The 1 μM ursolic acid (UA) could alleviate 8 μM ochratoxin A (OTA) nephrotoxicity. • The 1 μM UA could alleviate 8 μM OTA-induced ROS production. • Ameliorative effect of UA on OTA nephrotoxicity was mediated by Lonp1/Aco2/Hsp75. [ABSTRACT FROM AUTHOR]